The metabolic alterations in tumor cells are mainly driven by aberrant activation of the phosphatidylinositol-3 kinase-protein kinase B-mammalian target of rapamycin (PI3K-AKT-mTOR) pathway and activation of oncogenes such as MYC, RAS, and hypoxia-inducible factor 1 (HIF-1), as well as mutations or deactivation of tumor suppressor genes including p53 and PTEN (phosphatase and tensin homolog) (Supplementary Box 1). The gene discussed is AKT1; the disease is neoplasm.